11. Glomerular Pathology Flashcards

1
Q

Where is the likely site of injury in proteinuria/nephrotic syndrome?

A

Podocyte or subepithelial damage.

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2
Q

What are the 3 most common primary causes of proteinuria/nephrotic syndrome?

A

Minimal change glomerulonephritis.
Focal segmental glomerulosclerosis.
Membranous glomerulonephritis.

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3
Q

Name 1 common secondary cause of proteinuria/nephrotic syndrome?

A

Diabetes mellitus.

Amyloidosis.

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4
Q

Which age group is minimal change glomerulonephritis most common in?

A

Childhood/adolescence.

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5
Q

What treatment does minimal change glomerulonephritis respond to?

A

Steroids (but may recur when steroids stopped).

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6
Q

Does minimal change glomerulonephritis usually progress to renal failure?

A

No, does not usually progress to renal failure.

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7
Q

How does the glomerulus look histologically in minimal change glomerulonephritis?

A

Glomerulus looks normal, but there are no podocytes visible as they have been damaged (cannot selectively filter proteins anymore).

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8
Q

What causes podocyte damage in minimal change glomerulonephritis?

A

An unknown circulating factor damages the podocytes. There is no immune complex deposition.

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9
Q

In which age group is focal segmental glomerulosclerosis more common?

A

Adults.

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10
Q

What causes podocyte damage in focal segmental glomerulosclerosis and what consequence does this have for treatment?

A

Circulating factor damages podocytes. FSGS is progressive to renal failure, but if the patient has a kidney transplant, the transplanted kidney will also get FSGS due to the circulating factors. So treatment is with dialysis rather than transplant.

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11
Q

Which age group if membranous glomerulonephritis most common in?

A

Adults.

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12
Q

How does membranous glomerulonephritis typically progress?

A

1/3 patients get better.
1/3 patients continue as they are.
1/3 patients progress to renal failure.

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13
Q

What causes podocyte damage in membranous glomerulonephritis?

A

Immune complex deposits against the podocytes - sub-epithelial deposits (so is probably autoimmune).

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14
Q

Is membranous glomerulonephritis primary or secondary?

A

Is primary but may be secondary as has been associated with other pathologies eg lymphoma.

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15
Q

What is seen histologically in patients with diabetes mellitus leading to nephrotic syndrome?

A

Mesangial sclerosis leading to nodules.

Basement membrane thickening.

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16
Q

Does nephrotic syndrome secondary to diabetes mellitus progress to renal failure?

A

Yes - progressive proteinuria and is progressive to renal failure.

17
Q

What are the two most common causes of haematuria?

A

IgA nephropathy.

Thin glomerular basement membrane disease/hereditary nephropathy (Alport).

18
Q

What are the two most common causes of nephritic syndrome?

A
Goodpasture syndrome (anti-GBM disease).
Vasculitis.
19
Q

In which age group os IgA nephropathy most common?

A

Any age group.

20
Q

What type of infections is IgA nephropathy associated with?

A

Mucosal infections - viral upper respiratory tract eg common cold.

21
Q

Does IgA nephropathy present with proteinuria?

A

It can present with or without proteinuria.

22
Q

Does IgA nephropathy progress to renal failure?

A

A significant proportion progress to renal failure.

23
Q

How would you treat a patient with IgA nephropathy?

A

There is no effective treatment.

24
Q

What is mesangial damage? Why does this occur and how does this lead to haematuria.

A

Loss of mesangial cells in the glomerulus.
Immune complexes (IgA) pass though the glomerulus to the mesangial cells causing damage.
Capillary loop becomes fragile, leading to haematuria.

25
Q

Name 2 heredity nephropathies that do not progress to renal failure.

A

Thin GBM nephropathy.
Benign familial nephropathy.
Isolated haematuria.
Thin GBM.

26
Q

Name 2 hereditary nephropathies that can progress to renal failure.

A
Alport.
X linked.
Abnormal collagen IV.
Associated with deafness.
Abnormal appearing GBM.
27
Q

Are hereditary nephropathies as clear cut as either progressive to renal failure or not progressive?

A

No, often a grey area of patients between the two types of conditions, likely to be because multiple genes make up the conditions.

28
Q

What is seen histologically in the glomerulus of patients with Alport’s syndrome?

A

Abnormally split and laminated GBM.

29
Q

Does goodpasture syndrome (anti-GBM) progress to renal failure?

A

Yes, is very rapidly progressive.

30
Q

How does goodpasture syndrome usually present?

A

Acute onset of severe nephritic syndrome, classically associated with pulmonary haemorrhage (smokers).

31
Q

What causes GBM damage in goodpasture syndrome?

A

Autoantibody to collage IV in basement membrane. IgG deposition, inflammation and necrosis, filter blocked, becomes nephritic and blood leaks out.

32
Q

How would you treat goodpasture syndrome if it is caught early?

A

Immunosuppresion and plasmaphoresis.

33
Q

What causes GBM damage in vasculitis?

A

Anti neutrophil cytoplasmic antibodies and neutrophils cause segmental necrosis by activating complement and so punching out holes in the GBM - endothelial damage.

34
Q

Is there immune complex/antibody deposition in vasculitis?

A

No - circulating antibodies to white cells.

35
Q

Is vasculitis treatable? What do you need to do urgently if you suspect a patient has vasculitis?

A

Only if caught early.

Urgent biopsy.

36
Q

How do patients with nephritic syndrome tend to present?

A

Hypertension.
Haematuria.
Oliguria.
Glomerular inflammation and reduction in GFR.

37
Q

How do patients with nephrotic syndrome tend to present?

A

Hypoalbuminemia.
Hyperlipidaemia.
Proteinuria.
Peripheral oedema.

38
Q

What conditions can present as either nephritic or nephrotic syndrome?

A

IgA purpura.
Post-infectious.
Lupus.

39
Q

How do patients with vasculitis tend to present?

A

Systemic symptoms - lungs affected (pulmonary-renal syndrome), fatigue, arthralgia, myalgia, weight loss.